RP - HPLC method for the estimation of Tamsulosin Hydrochloride in Tablet Dosage Form.

A rapid and sensitive reverse phase RP-HPLC method is proposed for the estimation of tamsulosin hydrochloride in tablets. Tamsulosin hydrochloride was chromatographed on a reverse phase C18 column with a mobile phase consisting of acetonitrile and water in the ratio of 50:50 v/v. The mobile phase was pumped at a flow rate of 1.

Human traumatic brain injury alters circulating L-arginine and its metabolite levels: possible link to cerebral blood flow, extracellular matrix remodeling, and energy status.

Altered cerebral blood flow, cell-matrix interactions, and energy metabolism are secondary pathologies contributing to outcome after traumatic brain injury (TBI). Because L-arginine serves as the precursor for metabolites that are critical to these processes, we measured their plasma levels using LC-MS/GC-MS. Samples were collected from healthy volunteers (n=20), and patients with mild TBI (n=18), severe TBI (n=20), or orthopedic injury without a TBI (n=15), within the first 24 hours of injury.

Involvement of the glycogen synthase kinase-3 signaling pathway in TBI pathology and neurocognitive outcome.

Background: Traumatic brain injury (TBI) sets in motion cascades of biochemical changes that result in delayed cell death and altered neuronal architecture. Studies have demonstrated that inhibition of glycogen synthase kinase-3 (GSK-3) effectively reduces apoptosis following a number of stimuli. The Wnt family of proteins, and growth factors are two major factors that regulate GSK-3 activity.

Quantitative impact of thymic selection on Foxp3+ and Foxp3- subsets of self-peptide/MHC class II-specific CD4+ T cells.

It is currently thought that T cells with specificity for self-peptide/MHC (pMHC) ligands are deleted during thymic development, thereby preventing autoimmunity. In the case of CD4(+) T cells, what is unclear is the extent to which self-peptide/MHC class II (pMHCII)-specific T cells are deleted or become Foxp3(+) regulatory T cells. We addressed this issue by characterizing a natural polyclonal pMHCII-specific CD4(+) T-cell population in mice that either lacked or expressed the relevant antigen in a ubiquitous pattern.

HIV-1 infection induces acetylation of NPM1 that facilitates Tat localization and enhances viral transactivation.

Human immunodeficiency virus type 1 (HIV-1) following integration hijacks host cell machineries where chromatinization of the viral genome regulates its latency, transcription, and replication. The cooperation among ATP-dependent chromatin remodeling factors, posttranslational modifying enzymes, and histone chaperones is well established during transcriptional activation in eukaryotes. However, the role of histone chaperones in transcription of the HIV promoter is poorly understood.

Clonally related CD8+ T cells responsible for rapid population of both diffuse nasal-associated lymphoid tissue and lung after respiratory virus infection.

The immune system has evolved to use sophisticated mechanisms to recruit lymphocytes to sites of pathogen exposure. Trafficking pathways are precise. For example, lymphocytes that are primed by gut pathogens can, in some cases, be imprinted with CCR9 membrane receptors, which can influence migration to the small intestine.

Adult skeletal muscle stem cell migration is mediated by a blebbing/amoeboid mechanism.

Adult skeletal muscle possesses a resident stem cell population called satellite cells, which are responsible for tissue repair following damage. Satellite cell migration is crucial in promoting rapid tissue regeneration, but it is a poorly understood process. Furthermore, the mechanisms facilitating satellite cell movement have yet to be elucidated.

A novel strategy to activate cytoprotective genes in the injured brain.

The transcription factor nuclear factor E2-related factor 2 (Nrf2) regulates the expression of multiple cytoprotective genes that have been shown to offer protection in response to a number of insults. The present study describes a novel strategy to increase expression of Nrf2-responsive genes in brain injured mice. Under normal conditions, the adapter protein Kelch-like ECH-associated protein 1 (Keap1) binds to Nrf2 and promotes its proteosomal degradation in the cytoplasm.

Comparative complete genome analysis of dengue virus type 3 circulating in India between 2003 and 2008.

Dengue is endemic in most parts of the tropics including India. So far, complete genome information for Indian dengue isolates is not available. In the present study, we characterized the genome of three dengue type 3 viruses isolated from India.

HIV-1 Tat-mediated induction of platelet-derived growth factor in astrocytes: role of early growth response gene 1.

HIV-associated neurologic disorders (HAND) are estimated to affect almost 60% of HIV-infected individuals. HIV encephalitis, the pathologic correlate of the most severe form of HAND, is often characterized by glial activation, cytokine-chemokine dysregulation, and neuronal damage and loss. However, the severity of HIV encephalitis correlates better with glial activation rather than viral load.

Multiple coregulatory control of tyrosine hydroxylase gene transcription.

Despite ubiquitous expression and a high level of metastasis-associated protein 1 (MTA1) coregulator, the physiological role of the MTA1 coactivator remains unknown. We found that MTA1 is a bona fide coactivator and stimulator of tyrosine hydroxylase (TH) transcription in neuronal cells and that MTA1-null mice had lower TH expression in the striatum and substantial nigra. MTA1 physically achieves these functions by interacting directly with DJ1 (Parkinson disease 7) and in turn recruits the DJ1/MTA1/RNA polymerase II complex to the bicoid binding element (BBE) in the TH promoter.

Loss of neuronal integrity during progressive HIV-1 infection of humanized mice.

Neuronal damage induced by ongoing human immunodeficiency virus type 1 (HIV-1) infection was investigated in humanized NOD/scid-IL-2Rγ(c)(null) mice transplanted at birth with human CD34-positive hematopoietic stem cells. Mice infected at 5 months of age and followed for up to 15 weeks maintained significant plasma viral loads and showed reduced numbers of CD4(+) T-cells. Prospective serial proton magnetic resonance spectroscopy tests showed selective reductions in cortical N-acetyl aspartate in infected animals.

Evaluation of a commercial Dengue NS1 enzyme-linked immunosorbent assay for early diagnosis of dengue infection.

Purpose: Dengue is one of the most serious mosquito-borne viral infections affecting tropical and subtropical countries in the world. Since there is no immunoprophylactic or specific antiviral therapy available, timely and rapid diagnosis plays a vital role in patient management and implementation of control measures. This paper evaluates a commercially available NS1 antigen capture ELISA vis-a-vis SD bioline Dengue NS1 antigen test for early detection of dengue virus.

Altered expression of miRNA-21 and its targets in the hippocampus after traumatic brain injury.

Traumatic brain injury (TBI) initiates many different signaling cascades throughout the brain that impact both pathophysiological and neuroprotective processes. Cellular mechanisms that can modulate these processes may play an important role in determining the nature and extent of the damage suffered after TBI and therefore influence overall outcome after injury. MicroRNAs (miRNAs) are an important class of noncoding regulatory RNAs providing an epigenetic mechanism for the regulation of protein expression levels of target genes.

Carnauba wax nanoparticles enhance strong systemic and mucosal cellular and humoral immune responses to HIV-gp140 antigen.

Induction of humoral responses to HIV at mucosal compartments without inflammation is important for vaccine design. We developed charged wax nanoparticles that efficiently adsorb protein antigens and are internalized by DC in the absence of inflammation. HIV-gp140-adsorbed nanoparticles induced stronger in vitro T-cell proliferation responses than antigen alone.

Paired analysis of TCRα and TCRβ chains at the single-cell level in mice.

Characterizing the TCRα and TCRβ chains expressed by T cells responding to a given pathogen or underlying autoimmunity helps in the development of vaccines and immunotherapies, respectively. However, our understanding of complementary TCRα and TCRβ chain utilization is very limited for pathogen- and autoantigen-induced immunity. To address this problem, we have developed a multiplex nested RT-PCR method for the simultaneous amplification of transcripts encoding the TCRα and TCRβ chains from single cells.

T Cell receptor clonotype influences epitope hierarchy in the CD8+ T cell response to respiratory syncytial virus infection.

CD8+ T cell responses are important for recognizing and resolving viral infections. To better understand the selection and hierarchy of virus-specific T cell responses, we compared the T cell receptor (TCR) clonotype in parent and hybrid strains of respiratory syncytial virus-infected mice. K(d)M2(82-90) (SYIGSINNI) in BALB/c and D(b)M(187-195) (NAITNAKII) in C57Bl/6 are both dominant epitopes in parent strains but assume a distinct hierarchy, with K(d)M2(82-90) dominant to D(b)M(187-195) in hybrid CB6F1/J mice.

Detection of dengue virus.

Global incidence of dengue has increased considerably over the past decade. Dengue fever (DF) is a self-limiting disease; however, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) are fatal. Since there is no therapy and vaccine against dengue, timely diagnosis is therefore necessary for patient management.

Clinical and molecular characterization of β(S) and (G)γ((A)γδβ)⁰-thalassemia in eastern India.

Fetal hemoglobin (Hb F) is the most studied modifier of sickle cell disease. Coinheritance of high Hb F determinants such as δβ-thalassemia (δβ-thal) and hereditary persistence of fetal hemoglobin (HPFH) can contribute to raised Hb F concentration in these patients. One hundred and seventy-six cases of sickle cell disease with high Hb F were screened for the presence of the Asian Indian deletion-inversion (G)γ((A)γδβ)⁰-thal and HPFH-3 (Indian, 48.

β-globin gene haplotypes linked with the Hb D-Punjab [β121(GH4)Glu→Gln, GAA>CAA] mutation in eastern India.

Hb D-Punjab [β121(GH4)Glu→Gln] is prevalent in the northern states of the Indian subcontinent. Due to inadequate data from Asian countries, the origin and spread of the Hb D-Punjab mutation are uncertain. In a study of sickle cell hemoglobinopathies, we detected the Hb D-Punjab mutation in 25 subjects from 11 unrelated Agharia families.

Altered adrenergic receptor signaling following traumatic brain injury contributes to working memory dysfunction.

The prefrontal cortex is highly vulnerable to traumatic brain injury (TBI) and its structural and/or functional alterations as a result of TBI can give rise to persistent working memory (WM) dysfunction. Using a rodent model of TBI, we have described profound WM deficits following TBI that are associated with increases in prefrontal catecholamine (both dopamine and norepinephrine) content. In this study, we examined if enhanced norepinephrine signaling contributes to TBI-associated WM dysfunction.

Human traumatic brain injury alters plasma microRNA levels.

Circulating microRNAs (miRNAs) present in the serum/plasma are characteristically altered in many pathological conditions, and have been employed as diagnostic markers for specific diseases. We examined if plasma miRNA levels are altered in patients with traumatic brain injury (TBI) relative to matched healthy volunteers, and explored their potential for use as diagnostic TBI biomarkers. The plasma miRNA profiles from severe TBI patients (Glasgow Coma Scale [GCS] score ≤8) and age-, gender-, and race-matched healthy volunteers were compared by microarray analysis.